JBNB  Vol.3 No.4 , October 2012
Pharmacogenomics: The Significance of Genetics in the Metabolism of Natural Medicines
Author(s) Nancy W. Hanna*
ABSTRACT
Natural products have been implemented in medicine through use as herbal medications, chemical compound extraction for prescription medication, or a natural source of food to fight various infections and diseases. Genetics has played a role in identifying various interactions between existing drugs and side effects. In addition, various food allergies have been identified with children in recent years, suggesting genetic associations between certain populations carrying specific genetic alleles. The recent availability of genomic data and our increased understanding of the effects of genetic variations permit a quantitative examination of the contribution of genetic variation to efficacy or toxicity of compounds derived from natural sources. The identification of target molecules relevant for diseases allows screening for natural products capable of inhibiting targets which can lead to the development of rational treatment of various diseases including neurobiological disorders, cancer, osteoporosis, and cardiovascular diseases. This allows for more opportunities to predict the response of individual patients. Identification of genetic variations that arose as a consequence of naturally occurring compounds will help identify gene alleles, or protein ligands that can affect the pharmacodynamic and pharmacokinetics of the natural products in question. In addition, diet modification and precautions to food products can be identified to help consumers limit or increase certain food intake. Understanding the molecular mechanisms underlying these interactions and their modification by genetic variation is expected to result in the development of new drugs that optimize individual health. We expect that strategies for individualized therapies will lead to improved results for patients.

Cite this paper
N. Hanna, "Pharmacogenomics: The Significance of Genetics in the Metabolism of Natural Medicines," Journal of Biomaterials and Nanobiotechnology, Vol. 3 No. 4, 2012, pp. 452-461. doi: 10.4236/jbnb.2012.34046.
References
[1]   I. S. Vizirianakis, “Improving Pharmacotherapy Outcomes by Pharmacogenomics: From Expectation to Reality?” Pharmacogenomics, Vol. 6, No. 7, 2005, pp. 701-711. doi:10.2217/14622416.6.7.701

[2]   U. Mahlknecht and S. Voelter-Mahlknecht, “Pharmacogenomics: Questions and Concerns,” Current Medical Research and Opinion, Vol. 21, No. 7, 2005, pp. 1041-1047. doi:10.1185/030079905X50633

[3]   H.-F. Ji, X.-J. Li and H.-Y. Zhang, “Natural Products and Drug Discovery,” EMBO Reports, Vol. 10, No. 3, 2009, pp. 194-200. doi:10.1038/embor.2009.12

[4]   P. Vuorelaa, et al., “Natural Products in the Process of Finding New Drug Candidates,” Current Medicinal Chemistry, Vol. 11, No. 11, 2004, pp. 1375-1389.

[5]   C.-W. Yeh, et al., “Suppression of Fatty Acid Synthase in MCF-7 Breast Cancer Cells by Tea and Tea Poly-phenols: A Possible Mechanism for Their Hypolipidemic Effects,” The Pharmacogenomics Journal, Vol. 3, 2003, pp. 267- 276.

[6]   N. Chalabi, et al., “Gene Signature of Breast Cancer Cell Lines Treated with Lycopene,” Pharmacogenomics, Vol. 7, No. 5, 2006, pp. 663-672. doi:10.2217/14622416.7.5.663

[7]   P. S. Rai, et al., “Genetic Variation in Genes Involved in Folate and Drug Metabolism in a South Indian Population,” Indian Journal of Human Genetics, Vol. 17, No. 1, 2011, pp. 48-53.

[8]   C. M. Ulrich, et al., “Pharmacogenetics and Folate Metabolism—A Promising Direction,” Pharmacogenomics, Vol. 3, No. 3, 2002, pp. 299-313. doi:10.1517/14622416.3.3.299

[9]   M. Krajinovic, et al., “Role of Polymorphisms in MTHFR and MTHFD1 Genes in the Outcome of Childhood Acute Lymphoblastic Leukemia,” The Pharmacogenomics Journal, Vol. 4, 2004, pp. 66-72. doi:10.1038/sj.tpj.6500224

[10]   D. E. Riechers and P. T. Michael, “Structure and Expression of the Gene Family Encoding Putrescine N-Methyl-transferase in Nicotiana Tabacum: New Clues to the Evolutionary Origin of Cultivated Tobacco,” Plant Molecular Biology, Vol. 41, No. 3, 1999, pp. 387-401. doi:10.1023/A:1006342018991

[11]   A. Rigbi, et al., “Why Do Young Women Smoke? VI. A Controlledstudy of Nicotine Effects on Attention: Pharmacogenetic Interactions,” The Pharmacogenomics Journal, Vol. 11, No. 1, 2011, pp. 45-52. doi:10.1038/tpj.2010.15

[12]   A. Rossini, et al., “CYP2A6 Polymorphisms and Risk for Tobacco-Related Cancers,” Pharmacogenomics, Vol. 9, No. 11, 2008, pp. 1737-1752. doi:10.2217/14622416.9.11.1737

[13]   J. K. Yano, et al., “Structures of Human Microsomal Cytochrome P450 2A6 Complexed with Coumarin and Methoxsalen,” Nature Structural and Molecular Biology, Vol. 12, No. 9, 2005, pp. 822-823. doi:10.1038/nsmb971

[14]   T. Errerth, et al., “Pharmacogenomics of a Traditional Japanese Herbal Medicine (Kampo) for Cancer Therapy,” Cancer Genomics and Proteomics, Vol. 4, 2007, pp. 81-92.

[15]   X. Chen, et al., Shikonin, a Component of Chinese Herbal Medicine, Inhibits Chemokine Receptor Function and Suppresses Human Immunodeficiency Virus Type 1,” Antimicrob Agents Chemother, Vol. 47, No. 9, 2003, pp. 2810-2816. doi:10.1128/AAC.47.9.2810-2816.2003

[16]   Y. Yuan and E. Q. Zhou, “A Novel Antiestrogen Agent Shikonin Inhibits Estrogen-Dependent Gene Transcription in Human Breast Cancer Cells,” Breast Cancer Research and Treatment, Vol. 121, No. 1, 2010, pp. 233-240. doi:10.1007/s10549-009-0547-2

[17]   S. Blum, et al., “Vitamin E Reduces Cardiovascular Disease in Individuals with Diabetes Mellitus and the Haptoglobin 2-2 Genotype,” Pharmacogenomics, Vol. 11, No. 5, 2010, pp. 675-684. doi:10.2217/pgs.10.17

[18]   A. P. Levy and S. Blum, “Pharmacogenomics in Prevention of Diabetic Cardiovascular Disease: Utilization of the Haptoglobin Genotype in Determining Benefit from Vitamin E,” Expert Review of Cardiovascular Therapy, Vol. 5, No. 6, 2007, pp. 1105-1111. doi:10.1586/14779072.5.6.1105

[19]   P. N. Mimche, et al., “The Plant-Based Immunomodulator Curcumin as a Potential Candidate for the Development of an Adjunctive Therapy for Cerebral Malaria,” Malaria Journal, Vol. 10, No. 1, 2011, pp. 1-9. doi:10.1186/1475-2875-10-S1-S10

[20]   Q. H. Kang and A. P. Chen. “Curcumin Eliminates Oxidized LDL Roles in Activating Hepatic Stellate Cells by Suppressing Gene Expression of Lectin-Like LDL Receptor-1,” Laboratory Investgation, Vol. 89, No. 11, 2009, pp. 1275-1290. doi:10.1038/labinvest.2009.93

[21]   J. A. Riancho, “Polymorphisms in the CYP19 Gene that Influence Bone Mineral Density,” Pharmacogenomics, Vol. 8, No. 4, 2007, pp. 339-352. doi:10.2217/14622416.8.4.339

[22]   S. C. Blum, et al., “Dietary Soy Protein Maintains Some Indices of Bone Mineral Density and Bone Formation in Aged Ovaricetomized Rats,” The Journal of Nutrition, Vol. 133, No. 5, 2003, pp. 1244-1249.

[23]   L. Gennari, et al., “Update on the Pharmacogenetics of the Vitamin D Receptor and Osteoporosis,” Pharmacogenomics, Vol. 10, No. 3, 2009, pp. 417-433. doi:10.2217/14622416.10.3.417

[24]   F. Massart, “Human Races and Pharmacogenomics of Effective Bone Treatments,” Gynecological Endocrinology, Vol. 20, No. 1, 2005, pp. 36-44. doi:10.1080/09513590400019437

[25]   C. A. Shively, et al., “Soy and Social Stress Affect Serotonin Neurotransmission in Primates,” The Pharmacogenomics Journal, Vol. 3, No. 2, 2003, pp. 114-121. doi:10.1038/sj.tpj.6500166

[26]   T. Hiroi, et al., “Protracted Lithium Treatment Protects against the ER Stress Elicited by Thapsigargin in Rat PC12 Cells: Roles of Intracellular Calcium, GRP78 and Bcl-2,” The Pharmacogenomics Journal, Vol. 5, 2005, pp. 102-111.

[27]   S. K. Kulkarni and A. Dhir, “An Overview of Curcumin in Neurological Disorders,” Indian Journal of Pharmaceutical Sciences, Vol. 72, No. 2, 2010, pp. 149-154. doi:10.4103/0250-474X.65012

[28]   S. Kulkarni, et al., “Anti-depressant Activity of Curcumin: Involvement of Serotonin and Dopamine System,” Psychopharmacology, Vol. 201, No. 3, 2008, pp. 435-442. doi:10.1007/s00213-008-1300-y

[29]   E. Erichorn, et al., “Digoxin—New Perspective on an Old Drug,” The New England Journal of Medicine, Vol. 347, No. 18, 2002, pp. 1394-1395. doi:10.1056/NEJMp020118

[30]   C. Verstuyft, et al., “Digoxin Pharmacokinetics and MD R1 Genetic Polymorphisms,” European Journal of Clinical Pharmacology, Vol. 58, No. 12, 2003, pp. 809-812.

[31]   G. D. Leschziner, et al., “ABCB1 Genotype and PGP Expression, Function and Therapeutic Drug Response: A Critical Review and Recommendations for Future Research,” The Pharmacogenomics Journal, Vol. 7, No. 3, 2007, pp. 154-179. doi:10.1038/sj.tpj.6500413

[32]   T. Sakaeda, et al., “Pharmacogenetics of MDR1 and Its Impact on the Pharmacokinetics and Pharmacodynamics of Drugs,” Pharmacogenomics, Vol. 4, No. 4, 2003, pp. 397-410. doi:10.1517/phgs.4.4.397.22747

[33]   N. W. Paul and A. D. Roses, “Pharmacogenetics and Pharmacogenomics: Recent Developments, Their Clinical Relevance and Some Ethical, Social, and Legal Implications,” Journal of Molecular Medicine, Vol. 81, No. 3, 2003, pp. 135-140.

 
 
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